ArticleBMC pregnancy and childbirth2025
Role of HMGB1 on the onset of preeclampsia.
Article in BMC pregnancy and childbirth, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Development and internal validation of a nomogram for predicting adverse pregnancy outcomes in women with early-onset preeclampsia.Frontiers in medicine · 2026Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe molecular mechanisms differentiating early-onset preeclampsia (EO-PE) from late-onset preeclampsia (LO-PE) remain unclear. High Mobility Group Box 1 (HMGB1), a pro-inflammatory cytokine involved in immune responses and oxidative stress, has emerged as a potential contributor to PE pathogenesis. Our aim was to investigate expression of HMGB1 in the placentas of EO- and LO-PE patients by immunohistochemical methods and in silico analysis.
methodsThis experimental case-control study included 20 EO-PE, 20 LO-PE, and 20 normotensive control pregnant women. Placental samples underwent immunohistochemical staining to determine HMGB1 expression levels, which were analyzed semiquantitatively using ImageJ software. Bioinformatic analysis utilizing STRING and Cytoscape identified HMGB1-associated protein networks and pathways relevant to PE. Clinical and biochemical parameters were statistically analyzed.
resultsHMGB1 expression was significantly elevated in placentas from EO-PE patients compared to both LO-PE and control groups (p < 0.05). Histopathological assessment indicated severe structural disruptions in EO-PE placentas, including increased fibrin deposition, vascular degeneration, and higher incidence of apoptotic cells. Bioinformatics revealed significant interactions of HMGB1 with cytokine signaling pathways (IL-4, IL-13, IL-10) and platelet-related pathways (platelet activation and aggregation). Clinically, EO-PE patients exhibited higher systemic inflammatory markers (CRP, WBC, NLR) and greater biochemical evidence of multi-organ dysfunction.
conclusionsThis study identifies significantly increased HMGB1 placental expression predominantly in EO-PE, supporting its role in heightened inflammation and endothelial dysfunction characteristic of this subgroup, suggesting its potential as a biomarker and therapeutic target specifically for EO-PE.
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